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Clemastine promotes recovery of neural function and suppresses neuronal apoptosis by restoring balance of pro-inflammatory mediators in an experimental model of intracerebral hemorrhage
- Source :
- International Journal of Medical Sciences
- Publication Year :
- 2020
-
Abstract
- Intracerebral hemorrhage (ICH) represents a common acute cerebrovascular event that imparts high rates of disability. The microglia-mediated inflammatory response is a critical factor in determining cerebral damage post-ICH. Clemastine (CLM) is a histamine receptor H1 (HRH1) antagonist that has been shown to modulate the inflammatory response. However, the effects of CLM on ICH and the underlying mechanism remain to be determined. This investigation reveals that CLM resulted in reduction of cerebral hematoma volume, decreased cerebral edema and lower rates of neuronal apoptosis as well as improved behavioral scores in an acute ICH murine model. CLM treatment was noted to decrease pro-inflammatory effectors and increased anti-inflammatory effectors post-ICH. In addition, CLM reduced the deleterious effects of activated microglia on neurons in a transwell co-culture system. Our findings show that CLM likely mediates its therapeutic effect through inhibition of microglia-induced inflammatory response and apoptosis, thereby enhancing restoration of neuronal function.
- Subjects :
- Male
histamine receptor H1
Primary Cell Culture
Apoptosis
Brain Edema
Pharmacology
Cerebral edema
Stereotaxic Techniques
03 medical and health sciences
Histamine receptor
Mice
0302 clinical medicine
medicine
Animals
Clemastine
cardiovascular diseases
Cells, Cultured
Cerebral Hemorrhage
Intracerebral hemorrhage
Neurons
Microglia
business.industry
Therapeutic effect
Antagonist
General Medicine
medicine.disease
Coculture Techniques
Disease Models, Animal
medicine.anatomical_structure
Neuroprotective Agents
030211 gastroenterology & hepatology
Inflammation Mediators
business
medicine.drug
Research Paper
Subjects
Details
- ISSN :
- 14491907
- Volume :
- 18
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- International journal of medical sciences
- Accession number :
- edsair.doi.dedup.....9b31068711961a348da581c8d4db03fe